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Genome Maintenance and Cancer
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Genome Maintenance and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 21031

Special Issue Editor

Dr. Miroslav Chovanec

E-Mail Website
Guest Editor
Department of Genetics, Cancer Research Institute, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05 Bratislava, Slovakia
Interests: DNA damage; DNA repair; cancer; biomarker; targeted therapy; treatment personalization
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For many decades, genome instability has been recognized as a driving force for the development of cancer, and DNA repair systems as crucial factors ensuring the maintenance of genome stability and prevention of cancer. However, these systems also represent cancer treatment obstacles, particularly in the case of using treatment regimens for which the primary pharmacological target is a DNA molecule. Understandably, DNA repair inhibitors, either alone or in combination, are highly promising anticancer tools necessary for achieving higher curability and longer survival rates. Historically, DNA repair inhibitors (natural or small molecules, epigenetic changes by CpG methylation and miRNA, etc.) have most often been used within a synthetic lethality approach, where they target cancer cells defective in specific DNA repair system(s). Therefore, comprehensive information on the DNA repair efficiency of cancer cells has a strong prognostic and predictive value. Genome instability and the mutation burden in these cancer cells may also have such a value and be targeted in treatment. Collectively, DNA damage and DNA repair pathways are promising cancer biomarkers with high potential for use in personalized treatment approaches.

Authors are warmly invited to submit original research and review articles to this Special Issue which address the latest progress and current understanding of the role of DNA damage and repair in cancer.

Topics include, but are not limited to:

  • Role of genome instability in cancer
  • Prognostic value of genome instability
  • Use of DNA repair inhibitors in cancer treatment
  • Role of DNA repair variants in cancer incidence and treatment
  • Synthetic lethality based on the use of DNA repair inhibitors
  • Targeting of DNA repair by miRNA
  • Loss of DNA repair in cancer
  • Drug targeting of genome instability in cancer
  • DNA repair biomarkers
  • Role of genome instability and DNA repair in tumour mutation load

Dr. Miroslav Chovanec
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • apoptosis
  • DNA damage
  • DNA repair
  • DNA damage response
  • cell cycle
  • DNA repair inhibitors
  • personalized treatment
  • cancer biomarker
  • radiotherapy
  • chemotherapy
  • synthetic lethality
  • DNA repair gene variants
  • tumour mutation burden
  • carcinogenesis
  • mutagenesis

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Published Papers (5 papers)

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Research

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13 pages, 3010 KiB  
Article
SerpinB10, a Serine Protease Inhibitor, Is Implicated in UV-Induced Cellular Response
by Hajnalka Majoros, Barbara N. Borsos, Zsuzsanna Ujfaludi, Zoltán G. Páhi, Mónika Mórocz, Lajos Haracska, Imre Miklós Boros and Tibor Pankotai
Int. J. Mol. Sci. 2021, 22(16), 8500; https://doi.org/10.3390/ijms22168500 - 7 Aug 2021
Cited by 4 | Viewed by 2795
Abstract
UV-induced DNA damage response and repair are extensively studied processes, as any malfunction in these pathways contributes to the activation of tumorigenesis. Although several proteins involved in these cellular mechanisms have been described, the entire repair cascade has remained unexplored. To identify new [...] Read more.
UV-induced DNA damage response and repair are extensively studied processes, as any malfunction in these pathways contributes to the activation of tumorigenesis. Although several proteins involved in these cellular mechanisms have been described, the entire repair cascade has remained unexplored. To identify new players in UV-induced repair, we performed a microarray screen, in which we found SerpinB10 (SPB10, Bomapin) as one of the most dramatically upregulated genes following UV irradiation. Here, we demonstrated that an increased mRNA level of SPB10 is a general cellular response following UV irradiation regardless of the cell type. We showed that although SPB10 is implicated in the UV-induced cellular response, it has no indispensable function in cell survival upon UV irradiation. Nonetheless, we revealed that SPB10 might be involved in delaying the duration of DNA repair in interphase and also in S-phase cells. Additionally, we also highlighted the interaction between SPB10 and H3. Based on our results, it seems that SPB10 protein is implicated in UV-induced stress as a “quality control protein”, presumably by slowing down the repair process. Full article
(This article belongs to the Special Issue Genome Maintenance and Cancer)
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24 pages, 2908 KiB  
Article
Recombination and Pol ζ Rescue Defective DNA Replication upon Impaired CMG Helicase—Pol ε Interaction
by Milena Denkiewicz-Kruk, Malgorzata Jedrychowska, Shizuko Endo, Hiroyuki Araki, Piotr Jonczyk, Michal Dmowski and Iwona J. Fijalkowska
Int. J. Mol. Sci. 2020, 21(24), 9484; https://doi.org/10.3390/ijms21249484 - 13 Dec 2020
Cited by 5 | Viewed by 3241
Abstract
The CMG complex (Cdc45, Mcm2–7, GINS (Psf1, 2, 3, and Sld5)) is crucial for both DNA replication initiation and fork progression. The CMG helicase interaction with the leading strand DNA polymerase epsilon (Pol ε) is essential for the preferential loading of Pol ε [...] Read more.
The CMG complex (Cdc45, Mcm2–7, GINS (Psf1, 2, 3, and Sld5)) is crucial for both DNA replication initiation and fork progression. The CMG helicase interaction with the leading strand DNA polymerase epsilon (Pol ε) is essential for the preferential loading of Pol ε onto the leading strand, the stimulation of the polymerase, and the modulation of helicase activity. Here, we analyze the consequences of impaired interaction between Pol ε and GINS in Saccharomyces cerevisiae cells with the psf1-100 mutation. This significantly affects DNA replication activity measured in vitro, while in vivo, the psf1-100 mutation reduces replication fidelity by increasing slippage of Pol ε, which manifests as an elevated number of frameshifts. It also increases the occurrence of single-stranded DNA (ssDNA) gaps and the demand for homologous recombination. The psf1-100 mutant shows elevated recombination rates and synthetic lethality with rad52Δ. Additionally, we observe increased participation of DNA polymerase zeta (Pol ζ) in DNA synthesis. We conclude that the impaired interaction between GINS and Pol ε requires enhanced involvement of error-prone Pol ζ, and increased participation of recombination as a rescue mechanism for recovery of impaired replication forks. Full article
(This article belongs to the Special Issue Genome Maintenance and Cancer)
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Review

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22 pages, 2693 KiB  
Review
Detection of Genomic Uracil Patterns
by Angéla Békési, Eszter Holub, Hajnalka Laura Pálinkás and Beáta G. Vértessy
Int. J. Mol. Sci. 2021, 22(8), 3902; https://doi.org/10.3390/ijms22083902 - 9 Apr 2021
Cited by 6 | Viewed by 3937
Abstract
The appearance of uracil in the deoxyuridine moiety of DNA is among the most frequently occurring genomic modifications. Three different routes can result in genomic uracil, two of which do not require specific enzymes: spontaneous cytosine deamination due to the inherent chemical reactivity [...] Read more.
The appearance of uracil in the deoxyuridine moiety of DNA is among the most frequently occurring genomic modifications. Three different routes can result in genomic uracil, two of which do not require specific enzymes: spontaneous cytosine deamination due to the inherent chemical reactivity of living cells, and thymine-replacing incorporation upon nucleotide pool imbalances. There is also an enzymatic pathway of cytosine deamination with multiple DNA (cytosine) deaminases involved in this process. In order to describe potential roles of genomic uracil, it is of key importance to utilize efficient uracil-DNA detection methods. In this review, we provide a comprehensive and critical assessment of currently available uracil detection methods with special focus on genome-wide mapping solutions. Recent developments in PCR-based and in situ detection as well as the quantitation of genomic uracil are also discussed. Full article
(This article belongs to the Special Issue Genome Maintenance and Cancer)
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18 pages, 2002 KiB  
Review
Palindromes in DNA—A Risk for Genome Stability and Implications in Cancer
by Marina Svetec Miklenić and Ivan Krešimir Svetec
Int. J. Mol. Sci. 2021, 22(6), 2840; https://doi.org/10.3390/ijms22062840 - 11 Mar 2021
Cited by 14 | Viewed by 7213
Abstract
A palindrome in DNA consists of two closely spaced or adjacent inverted repeats. Certain palindromes have important biological functions as parts of various cis-acting elements and protein binding sites. However, many palindromes are known as fragile sites in the genome, sites prone to [...] Read more.
A palindrome in DNA consists of two closely spaced or adjacent inverted repeats. Certain palindromes have important biological functions as parts of various cis-acting elements and protein binding sites. However, many palindromes are known as fragile sites in the genome, sites prone to chromosome breakage which can lead to various genetic rearrangements or even cell death. The ability of certain palindromes to initiate genetic recombination lies in their ability to form secondary structures in DNA which can cause replication stalling and double-strand breaks. Given their recombinogenic nature, it is not surprising that palindromes in the human genome are involved in genetic rearrangements in cancer cells as well as other known recurrent translocations and deletions associated with certain syndromes in humans. Here, we bring an overview of current understanding and knowledge on molecular mechanisms of palindrome recombinogenicity and discuss possible implications of DNA palindromes in carcinogenesis. Furthermore, we overview the data on known palindromic sequences in the human genome and efforts to estimate their number and distribution, as well as underlying mechanisms of genetic rearrangements specific palindromic sequences cause. Full article
(This article belongs to the Special Issue Genome Maintenance and Cancer)
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12 pages, 12916 KiB  
Review
The Multiple Cellular Roles of SMUG1 in Genome Maintenance and Cancer
by Sripriya Raja and Bennett Van Houten
Int. J. Mol. Sci. 2021, 22(4), 1981; https://doi.org/10.3390/ijms22041981 - 17 Feb 2021
Cited by 10 | Viewed by 2932
Abstract
Single-strand selective monofunctional uracil DNA glycosylase 1 (SMUG1) works to remove uracil and certain oxidized bases from DNA during base excision repair (BER). This review provides a historical characterization of SMUG1 and 5-hydroxymethyl-2′-deoxyuridine (5-hmdU) one important substrate of this enzyme. Biochemical and structural [...] Read more.
Single-strand selective monofunctional uracil DNA glycosylase 1 (SMUG1) works to remove uracil and certain oxidized bases from DNA during base excision repair (BER). This review provides a historical characterization of SMUG1 and 5-hydroxymethyl-2′-deoxyuridine (5-hmdU) one important substrate of this enzyme. Biochemical and structural analyses provide remarkable insight into the mechanism of this glycosylase: SMUG1 has a unique helical wedge that influences damage recognition during repair. Rodent studies suggest that, while SMUG1 shares substrate specificity with another uracil glycosylase UNG2, loss of SMUG1 can have unique cellular phenotypes. This review highlights the multiple roles SMUG1 may play in preserving genome stability, and how the loss of SMUG1 activity may promote cancer. Finally, we discuss recent studies indicating SMUG1 has moonlighting functions beyond BER, playing a critical role in RNA processing including the RNA component of telomerase. Full article
(This article belongs to the Special Issue Genome Maintenance and Cancer)
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